B. Chatterjee

Small molecule FICD inhibitors suppress endogenous and pathologic FICD-mediated protein AMPylation

This study identifies two small molecule inhibitors of FICD that suppress both endogenous and pathologic protein AMPylation, improving proinsulin processing in β cells.

Ellagic acid: a potential inhibitor of enhancer of zeste homolog-2 and protein arginine methyltransferase-5

This study identifies ellagic acid as an inhibitor of EZH2 and PRMT5:MEP50, showing reduced histone modifications and tumor growth in mouse models.

Epigallocatechin-3-gallate inhibit the protein arginine methyltransferase 5 and Enhancer of Zeste homolog 2 in breast cancer both in vitro and in vivo

This study shows that EGCG inhibits PRMT5 and EZH2 in breast cancer cells and xenografts, reducing histone repressive marks and inducing apoptosis and autophagy.

Epstein Barr virus infection induces tissue-resident memory T cells in mucosal lymphoid tissues

This study shows EBV infection induces tissue-resident memory T cells in mucosal lymphoid tissues in mice with humanized immune systems, but these TRMs fail to control viral loads compared to systemic effector memory T cells.

Long-term Hematopoietic Transfer of the Anti-Cancer and Lifespan-Extending Capabilities of A Genetically Engineered Blood System by Transplantation of Bone Marrow Mononuclear Cells

This study shows that bone marrow mononuclear cells from genetically engineered mice can transfer anti-cancer and lifespan-extending properties to wild-type mice.

Bi-Phasic Quasistatic Brain Communication for Fully Untethered Connected Brain Implants

This paper introduces BP-QBC, a new wireless communication method for brain implants that achieves low end-to-end channel loss and high data rates using electro-quasistatic signaling.

Bio-Physical Modeling of Galvanic Human Body Communication in Electro-Quasistatic Regime

This paper develops a detailed lumped element model for Galvanic Human Body Communication (HBC) to analyze channel loss factors like tissue properties, electrode configuration, and return path capacitance.

An epithelial Nfkb2 pathway exacerbates intestinal inflammation by supplementing latent RelA dimers to the canonical NF-κB module

The paper shows that noncanonical NF-κB signaling in intestinal epithelial cells enhances latent RelA dimers, amplifying canonical NF-κB activity and exacerbating intestinal inflammation in IBD.